Evidence map›Paper›PMID 32317964›Full record

ArticleFrontiers in pharmacology2020

Systems Pharmacology Approach to Investigate the Mechanism of Kai-Xin-San in Alzheimer's Disease.

Yunxia Luo, Dongli Li, Yanfang Liao, Chuipu Cai, Qihui Wu, Hanzhong Ke, Xinning Liu, Huilin Li, Honghai Hong, Yumin Xu and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 44 citations in OpenAlex.

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  19. DPHB, a diarylheptane fromFrontiers in pharmacology · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 2 countries.

Yunxia LuoScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
Dongli LiScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
Yanfang LiaoScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
Chuipu CaiScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
Qihui WuScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
Hanzhong KeDepartment of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, United States.
Xinning LiuScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
Huilin LiDepartment of Endocrinology, Fourth Clinical Medical College, Guangzhou University of Chinese Medicine, Shenzhen, China.
Honghai HongDepartment of Clinical Laboratory, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Yumin XuDepartment of Encephalopathy First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Qi WangScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
Jiansong FangScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
Shuhuan FangScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, China.
Guangzhou University of Chinese Medicine · CNFirst Affiliated Hospital of Henan University · CNHarvard University · USThird Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a complex neurodegenerative disease characterized by cognitive dysfunction. Kai-Xin-San (KXS) is a traditional Chinese medicine (TCM) formula that has been used to treat AD patients for over a thousand years in China. However, the therapeutic mechanisms of KXS for treating AD have not been fully explored. Herein, we used a comprehensive network pharmacology approach to investigate the mechanism of action of KXS in the treatment of AD. This approach consists of construction of multiple networks and Gene Ontology enrichment and pathway analyses. Furthermore, animal experiments were performed to validate the predicted molecular mechanisms obtained from the systems pharmacology-based analysis. As a result, 50 chemicals in KXS and 39 AD-associated proteins were identified as major active compounds and targets, respectively. The therapeutic mechanisms of KXS in treating AD were primarily related to the regulation of four pathology modules, including amyloid beta metabolism, tau protein hyperphosphorylation process, cholinergic dysfunction, and inflammation. In scopolamine-induced cognitive dysfunction mice, we validated the anti-inflammatory effects of KXS on AD by determining the levels of inflammation cytokines including interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α. We also found cholinergic system dysfunction amelioration of KXS is correlated with upregulation of the cholinergic receptor CHRNB2. In conclusion, our work proposes a comprehensive systems pharmacology approach to explore the underlying therapeutic mechanism of KXS for the treatment of AD.

Indexed as

Alzheimer's diseasecholinergic systemKai-Xin-Sanneuroinflammationsystems pharmacology

Identifiers

PMID32317964
PMCPMC7147119
OpenAlexW3014316815

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.